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오미자 활성성분 DDB의 NF-κB 신호 전달 및 염증물질 발현 조절.Regulation of Inflammatory Repertoires and NF-κB Signal Transduction by DDB, an Active Compound from Schizandra Chinensis Baillon

Authors
주성수유영민원태준김민정이선구황광우이도익
Issue Date
2006
Publisher
대한면역학회
Keywords
Nitric oxide; iNOS; NF-κB; IL-1β; biphenyl dimethyl dicarboxylate; alzheimer's disease
Citation
Immune Network, v.6, no.1, pp 27 - 32
Pages
6
Journal Title
Immune Network
Volume
6
Number
1
Start Page
27
End Page
32
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/29251
ISSN
1598-2629
2092-6685
Abstract
Background: Chronic inflammation in the brain has known to be associated with the development of a various neurological diseases including dementia. In general, the characteristic of neuro-inflammation is the activated microglia over the brain where the pathogenesis occurs. Pro-inflammatory repertoires, interleukin-1β (IL-1β) and nitric oxide (NO), are the main causes of neuro-degenerative disease, particularly in Alzheimer's disease (AD) which is caused by neuronal destruction. Those pro-inflammatory repertoires may lead the brain to chronic inflammatory status, and thus we hypothesized that chronic inflammation would be inhibited when pro-inflammatory repertoires are to be well controlled by inactivating the signal transduction associated with inflammation. Methods: In the present study, we examined whether biphenyl dimethyl dicarboxylate (DDB), an active compound from Schizandra chinensis Baillon, inhibits the NO production by a direct method using Griess reagent and by RT-PCR in the gene expression of inducible nitric oxide synthase (iNOS) and IL-1β. Western blots were also used for the analysis of NF-κB and IκB. Results: In the study, we found that DDB effectively inhibited IL-1β as well as NO production in BV-2 microglial cell, and the translocation of NF-κB was comparably inhibited in the presence of DDB comparing those to the positive control, lipopolysaccharide. Conclusion: The data suggested that the DDB from Schizandra chinensis Baillon may play an effective role in inhibiting the pro-inflammatory repertoires which may cause neurodegeneration and the results imply that the compound suppresses a cue signal of the microglial activation which can induce the brain pathogenesis such as Alzheimer's disease. (Immune Network 2006;6(1):27- 32)
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